A number of vascular grafts occlude after months and sometimes years of apparently normal function. Such occlusion has been observed particularly for small diameter prostheses, or prostheses joined to small diameter vessels. In many cases, a characteristic hyperplastic lesion of the arterial wall has been noted at, or just beyond, the distal anastomosis. Although hyperplasia may occur at both the proximal and distal junctions, its usual manifestation is occlusion at the distal anastomosis.
While it has been generally considered that anastomotic hyperplasia in the region of the distal anastomosis is a phenomonon of unknown etiology, it now appears that a number of factors act in concert to bring about the development of this condition.
In the conventional end-to-side anastomosis (i.e. where the end of a graft tube enters the side of a vessel), there are many sources of stress at or near the junction site, including the dimensional difference between graft and vessel, the nature of the end-to-side anastomosis, and the difference in mechanical properties between graft and vessel. All of these stresses appear to be contributing factors in the development of arterial wall hyperplasia. Abnormal shear stresses continuously act upon the endothelium, leading to potential endothelial disruption. Activated blood, emerging from the prosthesis, bathes the disrupted endothelium, with resultant rapid platelet deposition. Continuous platelet deposition is another powerful stimulant to arterial hyperplasia.
It appears that size discrepancy between the prosthesis and the smaller vessel, alone, produces significant wall stress. Most vascular surgeons typically join a prosthesis with an inside diameter larger than that of the artery to the edges of a longitudinal slit in the artery. For example, an 8 mm graft might be joined to an artery of only 4 to 5 mm, with the "goal" of opening the anastomosis as widely as possible (to avoid occlusion). In fact, this practice actually leads to increased wall tension, a factor which promotes occlusion. This increase in tension is evident by considering the Laplace Law (tension=pressure.times.radius of curvature). Thus, the tension in the arterial segment increases as the radius of curvature of the arterial segment increases. Wall tension increases dramatically when dealing with vessels of small diameter (3 to 6 mm) where the margins needed for sutures have a significant effect on the effective radius of curvature. The foregoing considerations lead to the following criteria for the construction of small diameter vascular bypass prostheses:
1. the prosthesis must minimize or eliminate any stress to the arterial wall; PA1 2. the normal flow patterns must be preserved; PA1 3. the activation of blood to rapid thrombus formation must be minimized.
It is an object of this invention to provide a new and improved small diameter vascular bypass system, and a method for properly installing it, that will minimize the occlusion of small diameter vascular systems, by incorporation of the above criteria.